| Project/Area Number |
22700407
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | National Center of Neurology and Psychiatry |
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Principal Investigator |
TOGASHI Kazuya 独立行政法人国立精神・神経医療研究センター, 神経研究所疾病研究第五部, 流動研究員 (40450613)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Na+/H+交換輸送体 / オートファジー / 神経変性疾患 |
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| Research Abstract |
Autophagy is an intracellular degradation process that clears long-lived proteins and organelles from the cytoplasm, and then maintains normal cellular functions. Thus failure of autophagy in neurons can result in the accumulation of aggregate-prone proteins and neurodegeneration. However, the regulation mechanism of autophagy in brain is less known. In the present study, I found that an NHE blocker inhibited autophagy and that the over expression of plasma membrane type NHEs significantly reduced the formation of poly glutamine aggregation in a cell-line. Moreover, NHE5KO/Htt-Tg mice were generated by crossing with NHE5 knockout mouse and a Huntington's disease model mouse in which a large number of aggregations were observed in the cerebellar granule cells.
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